Medical devices are implanted in patients to monitor, among other things, electrical activity of a heart and to deliver appropriate electrical and/or drug therapy, as required. Implantable medical devices (“IMDs”) include, for example, pacemakers, cardioverters, defibrillators, implantable cardioverter defibrillators (“ICD”), and the like. The electrical therapy produced by an IMD may include, for example, pacing pulses, cardioverting pulses, and/or defibrillator pulses to reverse arrhythmias (e.g., tachycardias and bradycardias) or to stimulate the contraction of cardiac tissue (e.g., cardiac pacing) to return the heart to its normal sinus rhythm. Certain types of arrhythmias are caused by ischemia.
Cardiac ischemia is a condition whereby the heart tissue does not receive adequate amounts of oxygen. Ischemia arises during angina, coronary angioplasty, and many other conditions that compromise blood flow to a region of heart tissue. When blockage of an artery is sufficiently severe, the cardiac ischemia may progress into an acute myocardial infarction (“AMI”), which also is referred to as a myocardial infarction (“MI”) or a heart attack. Cardiac ischemia and myocardial infarction are usually caused by blockage of an artery leading to the heart tissue. The heart will experience ischemia in different regions based on which artery experiences the blockage and where the blockage is along the artery. For example, anterior wall ischemia/infarction is generally due to blockage in the left anterior descending coronary artery. Occlusion of the proximal left anterior descending coronary artery above the first septal and first diagonal branches may cause ischemia/infarction in the basal portion of the left ventricle, as well as in the anterior and lateral walls and the interventricular septum.
Past studies have been conducted to interpret the results of electrocardiograph (ECG) signals that are collected by external devices that are connected to 12 leads attached to the chest and back of a patient. The ECG signals have been analyzed in an effort to diagnose ischemia and infarction. ECG changes, that are association with ischemia and infarction, include hyper acute T wave changes, ST segment elevation and/or depression, changes in QRS complex and inverted T waves. Changes in the ST segment may be produced by the flow of currents generated by voltage gradients across the boundary between ischemic and non-ischemic regions during the resting and plateau phases of the ventricular action potential which corresponds to the TQ and ST segments of the ECG signals.
When certain leads within an external ECG system detect substantial ST segment shifts, this may be an indicator of potential blockage in certain arteries. However, the conventional external ECG analysis has certain limitations. For example, the patient must be coupled to the external ECG system while the patient is experiencing ischemia. Not all types of ischemia persist permanently. When a non-physiologic event occurs, a local region or local regions of the heart, not previously in an ischemic state, may enter an ischemic state. The ischemic region progresses over a period of time following the non-physiologic event. For example, the ischemic region may grow or develop in a particular direction. After a period of time, regions that experience certain types of ischemia revert back to a normal non-ischemic state.
Conventional ECG systems may not be coupled to the patient at the time period following a non-physiologic event during which the region is ischemic. Further, when a conventional ECG system is connected to a patient while a region of the heart is in an ischemic state, the ECG system is unable to characterize the dynamic behavior of the ischemic region. For example, conventional external ECG systems are unable to identify i) changes in a size of an ischemic region, ii) a direction of the progression of the ischemic region, or iii) a rate at which the ischemic region progresses. Moreover, conventional external ECG systems are not able to provide quantitative information regarding the progression of an ischemic region from the time at which a non-physiologic event occurs until the ischemic region enters a stable persistent state or reverts to a non-ischemic state.
Many patients at risk of cardiac ischemia have pacemakers, ICDs or other medical devices implanted therein. The implanted device senses an intra-cardiac electrogram (“IEGM”). IEGMs are composed of various waves and segments that represent the heart depolarizing and repolarizing. The ST segment in an IEGM represents the portion of the cardiac signal between ventricular depolarization and ventricular repolarization. Deviation of the ST segment from a baseline is a result of injury to cardiac muscle, variations in the synchronization of ventricular muscle depolarization, drug or electrolyte influences, or the like. Techniques have been developed to identify the presence of cardiac ischemia using implanted medical devices by identifying variations in the ST segment from the baseline cardiac signal that occur during cardiac ischemia.
However, conventional implantable devices have not yet been able to differentiate between different types of ischemia. Not all ischemic events progress to the state of an AMI. Instead, some ischemic events may be characterized as transient ischemia, while other ischemic events represent persistent spreading ischemia. One difference between transient ischemia and spreading ischemia is that transient ischemia generally reverses, while spreading ischemia often leads to permanent cardiac tissue damage and an AMI. Therefore, a transient ischemic event may occur for a relatively short period of time (e.g., a few hours) and go undetected by an external ECG system, but may not persist, nor develop into an AMI.
It has been suggested that, when less than 5% of the myocardium tissue is in an ischemic state, this condition may not be clinically significant. However, when more than 10% of the myocardial tissue exhibits a transient ischemic state, then it may be appropriate for the clinician to intervene for treatment such as utilizing an angiogram, balloon catheter, stents or medication. Often transient ischemia goes away by itself without intervention.
A need remains for improved methods and systems to monitor ischemic events and differentiate transient ischemia from persistent spreading ischemia.